The time course of action potential repolarization affects delayed afterdepolarization amplitude in atrial fibers of the canine coronary sinus.

Henning, B; Wit, Andrew L.

doi:10.1161/01.res.55.1.110

Cited by 29 publications

(12 citation statements)

References 40 publications

(55 reference statements)

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“…In addition to the PVs, arrhythmic activity may also originate from "myocardial sleeves" in other atrial regions, such as myocardial extensions in the atrioventricular valves and coronary sinus (37, 267, 621-623). Wit and co-workers have amassed an extensive body of data on catecholamine-induced delayed afterdepolarizations (DADs) and triggered activity elicited by fast pacing or extrastimulation in the canine coronary sinus (232,566,621). DADs in coronary sinus myocytes involve Ca 2ϩ release from the sarcoplasmic reticulum (21) and activation of a transient inward current (565).…”

Section: Electrical Activity Of Myocardial Sleevesmentioning

confidence: 99%

Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal

Schotten

Verheule²,

Kirchhof³

et al. 2011

Physiological Reviews

1,059

919

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Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological alterations promoting AF have been studied extensively in animal models. Atrial tachycardia or AF itself shortens atrial refractoriness and causes loss of atrial contractility. Aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. These changes in electrical, contractile, and structural properties of the atria have been called "atrial remodeling." The resulting electrophysiological substrate is characterized by shortening of atrial refractoriness and reentrant wavelength or by local conduction heterogeneities caused by disruption of electrical interconnections between muscle bundles. Under these conditions, ectopic activity originating from the pulmonary veins or other sites is more likely to occur and to trigger longer episodes of AF. Many of these alterations also occur in patients with or at risk for AF, although the direct demonstration of these mechanisms is sometimes challenging. The diversity of etiological factors and electrophysiological mechanisms promoting AF in humans hampers the development of more effective therapy of AF. This review aims to give a translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process. We pay attention to translation of pathophysiological insights gained from in vitro experiments and animal models to patients. Also, suggestions for future research objectives and therapeutical implications are discussed.

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Section: Electrical Activity Of Myocardial Sleevesmentioning

confidence: 99%

Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal

Schotten

Verheule²,

Kirchhof³

et al. 2011

Physiological Reviews

1,059

919

View full text Add to dashboard Cite

show abstract

“…This type of proarrhythmia is called triggered activity, and may be caused by "early" and "late" afterdepolarizations [43,82,129,243]. Early afterdepolarizations are most common during drug-induced QT prolongation and occur as oscillations that interrupt phase 2 or phase 3 of the repolarization process of the AP.…”

Section: Dispersion Of Ventricular Repolarization and Cellular Excitamentioning

confidence: 99%

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

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The antiarrhythmic principle of drug-induced QT-interval prolongation is well known. However, with the widespread use of the presently known and new Class III antiarrhythmic agents under investigation, and the growing number of agents not primarily designed as antiarrhythmic drugs that potentially cause QT prolongation, we have also become aware of the proarrhythmic hazards associated with many of these agents. The proarrhythmic risk differs markedly from one agent to another and interferes with many individual clinical variables (e.g., hypokalemia, sinus bradycardia). This paper summarizes the present data on the proarrhythmic risk of drug-induced QT prolongation, including the value and problems of the rate-corrected QT interval, the mechanisms involved in the genesis of proarrhythmia, and the clinical cofactors that facilitate the occurrence of proarrhythmic events. In addition, an extensive database provides information on the known proarrhythmic risk of all currently used QT-prolonging agents.

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“…these conditions. Support for this view is provided by a study in fibers of the canine coronary sinus that showed that acceleration of repolarization decreased the amplitude of delayed afterdepolarizations (Henning and Wit, 1984). Another possibility is that increasing [Ca ++ ]o, even in the presence of ouabain, does not produce a monotonic increase in the level of myoplasmic Ca ++ in diabetic fibers.…”

Section: Effects Of Ouabain and Increasing External Calcium Concentramentioning

confidence: 99%

Delayed afterdepolarizations and triggered activity in ventricular muscle from rats with streptozotocin-induced diabetes.

Nordin¹,

Gilat

Aronson

1985

Circulation Research

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Previous studies have shown that myocardium of the diabetic rat has impaired myoplasmic calcium metabolism. Delayed afterdepolarizations and triggered activity are potentiated by conditions believed to increase intracellular calcium concentration therefore, we performed this study to investigate the possibility that myocardium of the diabetic rat is more susceptible than normal tissue to develop afterdepolarizations and triggered activity. We used standard microelectrode techniques to record the electrical activity of papillary muscles from hearts of control rats and rats made diabetic with streptozotocin. We compared the response of control and diabetic preparations to conditions presumed to create progressively more severe degrees of myoplasmic calcium loading, viz. perfusion with solutions containing ouabain (5 X 10(-5) M) and increasing concentrations of calcium (2.4, 4.8, 7.2, and 9.6 mM). Our results showed the following. Ventricular muscle from diabetic rats was more prone than normal myocardium to develop delayed afterdepolarizations and triggered activity under conditions believed to cause myoplasmic calcium overload. The external calcium concentration correlated with the incidence but not the magnitude or coupling interval of the delayed afterdepolarizations in fibers of diabetic rats. The action potentials in fibers of diabetic rats decreased markedly in duration after exposure to ouabain, whereas normal action potentials were not affected significantly; as external calcium was increased with ouabain still present, the action potential duration in diabetic fibers decreased slightly more, whereas the action potential duration in normal fibers did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

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The time course of action potential repolarization affects delayed afterdepolarization amplitude in atrial fibers of the canine coronary sinus.

Cited by 29 publications

References 40 publications

Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal

Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Delayed afterdepolarizations and triggered activity in ventricular muscle from rats with streptozotocin-induced diabetes.

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